We reported a case of cholangiocellular carcinoma with elevated serum AFP-L3 level. A 70-year-old man who complained of body weight loss was pointed out a liver tumor at a near doctor and refered to our hospital. A tumor of 7 cm in diameter and other small nodules were detected by abdominal dynamic CT and ultrasonography. HBsAg and anti HCV were negative. Slight elevation of AFP 63.6 ng/ml and PIVKA-II 46 mAU/ml were pointed out. On the other hand, CEA and CA19-9 were not elevated. We thought that hepatocellular carcinoma was higly suspected because of the remarkable elevation of AFP-L3 88.2%. But the tumor did not show typical tumor staining by dynamic CT and angiograpy. Histology of the tumor biopsy was poorly differentiated adenocarcinoma, and we diagnosed the tumor as cholangiocellular carcinoma because all possible origins were excluded. Systemic chemotherapy (5-FU+CDDP) was performed but discontinued because of adverse events. The patient died about 2 months after diagnosis. The elevation of AFP-L3 was thought to be specific to hepatocellular carcinoma, but differential diagnosis shoud be done carefully.

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The 69-year-old woman with a pancreatic cancer was admitted to our hospital due to dermal abscess which the cause bacillus was Serratia marcescens. She had received the PTC drainage for 17 months to reduce jaundice. Re-insertion of PTC tube and the drainage of dermal abscess improved obstructive jaundice temporarily. However, computed tomography revealed the formation of liver abscess with a diameter of 10 cm in which had much partition structure. The cause bacillus also was Serratia marcescens. Right anterior branch of portal vein penetrated liver abscess, differing from the picture of the usual bacterial liver abscess. This case is suggestive because Serratia marcescens infection may be critical for compromised patients.

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We previously reported three activated and two suppressed genes detected by cDNA microarrays in peripheral lymphocytes from chronic hepatitis C (C-CH) patients. In this report, we investigated whether they could predict the outcome of interferon (IFN) treatment. Ten C-CH patients were treated by β-interferon for 26 weeks (with some variations), and sustained virological response (SVR) was achieved in six. Three activated genes: migration inhibitory factor-related protein 14 (MRP-14), interleukin (IL)-8 precursor, and puromycin-sensitive aminopeptidase (PSA), were detected in 33%, 33% and 67%, respectively in SVR patients, and in 100%, 75% and 50%, respectively in non-SVR patients. Two suppressed genes, platelet basic protein (PBP). precursor and monoamine oxidase (MAO-A), were detected in 67% and 50%, respectively in SVR patients, but in 75% and 50%, respectively in non-SVR patients. Since the statistical analysis did not show significance in this small size pilot study, further study will be needed to prove the hypothesis that these genes would predict non-SVR in IFN teatment.

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